Abstract: Hebbian type, associative plasticity provides a cellular mechanism of learning and refinement of connectivity during development in a variety of biological systems. However, Hebbian learning rules introduce a positive feedback on changes of synaptic weights and neuronal activity, making learning systems prone to runaway dynamics. The need for mechanism(s) which constrain this tendency for runaway dynamics has been well-articulated by theoretical and modeling studies. However, biological basis of such mechanisms remains elusive.
In my talk I will consider an emerging view of synaptic weight changes as a result of mutual actions of different forms of plasticity playing distinct functional roles.
First, I will present experimental evidence for a novel form of heterosynaptic plasticity which accompany induction of Hebbian-type associative plasticity. This form of heterosynaptic plasticity requires raises of intracellular calcium concentration in the postsynaptic neuron, but does not require activity at the presynapse for the induction. It can be induced by conventional protocols used for the induction of associative plasticity, such as spike-timing dependent plasticity (STDP). It is weight-dependent: synapses with initially low release probability tend to potentiate, while synapses with initially high release probability tend to be depressed. I will consider how associative and heterosynaptic plasticity both shape synaptic weights.
Next, I will compare experimentally-observed properties of this form of plasticity to the requirements, which theoretical and modelling studies identified for the mechanisms maintaining synaptic homeostasis during on-going plastic changes driven by Hebbian-type learning. This comparison shows that weight-dependent heterosynaptic plasticity is a strong candidate to fulfill the homeostatic role.
Finally, I will present experimental evidence for modulation of heterosynaptic plasticity by adenosine, and consider how this modulation may switch the mode of operation of neurons between an unbalancing regime, which is dominated by associative plasticity and supports drastic changes of synaptic weights, and a homeostatic regime of tightly constrained synaptic changes.

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